ArticleClinical and experimental nephrology2019
Role of the putative PKC phosphorylation sites of the type IIc sodium-dependent phosphate transporter in parathyroid hormone regulation.
Article in Clinical and experimental nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Review
- Phosphate in Physiological and Pathological Mineralization: Important yet Often Unheeded.MedComm · 2025Review
- Tmem174, a regulator of phosphate transporter prevents hyperphosphatemia.Scientific reports · 2022Article
- Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients.BMC nephrology · 2020Article
- Insulin-like growth factor 1 modulates the phosphorylation, expression, and activity of organic anion transporter 3 through protein kinase A signaling pathway.Acta pharmaceutica Sinica. B · 2020Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundInjection of parathyroid hormone (PTH) rapidly stimulates renal Pi excretion, in part by downregulating NaPi-IIa (Npt2a/SLC34A1) and NaPi-IIc (Npt2c/SLC34A3) transporters. The mechanisms underlying the effects of PTH on NaPi-IIc are not fully elucidated.
methodsWe analyzed the effect of PTH on inorganic phosphate (Pi) reabsorption in Npt2a
resultsThe Npt2a
conclusionsThe present study suggests that acute regulation of NaPi-IIc protein by PTH is involved in the inactivation of Na
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Registered trials
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